There is no unifor m definition of anemia. The World Health Organization defines anemia as a hemoglobin (Hb) level less than 12 g/dL in adult women and less than 13 g/dL in adult men. These cutoffs are based on population data that did not include people > 65 years of age, and do not take into account the effect of race and ethnicity. From the NHANES III and the Scripps-Kaiser database, new lower limits of normal for men >59 years and women >49 years have been proposed after excluding those with confounding factors. These values were slightly higher for older white men and women (13.2 and 12.2 g/dL, respectively) and slightly lower for older black men and women (12.7 and 11.5, respectively). However, such levels may not be optimal with regard to morbidity and mortality. For example, in the Women’s Health and Aging Study, a risk gradient for adverse outcomes (mortality, frailty, disability) was present with Hb in the “normal range” as was a rise in the erythropoietin level [8]. In a multi-facility study, 56 % of residents were anemic; prior estimates have ranged from 25 to 63 % [9].

Signs and symptoms in long-term c are residents may be nonspecific (Table 4) so staff needs to be aware of their potential significance and report them to the practitioner.

Anemia is ge nerally due to an underlying clinical disorder and warrants an evaluation unless the resident has a reduced life expectancy, is receiving palliative care, or declines further evaluation. A systematic evaluation can help the practitioner make rational treatment decisions. Using empiric iron replacement, for example, can potentially overlook a significant underlying treatable disorder. The causes of anemia may be classified by etiology, bearing in mind that more than one cause may be present in a given person.

However, an alternative approach to aide clinical decision-making can be more useful in most clinical settings. It includes assessing the resident’s medical history, comorbidities, renal function, current and recent medication use, physical findings, and review of laboratory tests. Anemia can then be classified by considering kinetics (decreased production, increased destruction, or blood loss), or by considering red cell morphology. The following algorithm (Fig. 1) suggests a diagnostic approach using the corrected reticulocyte count and MCV (as low, normal, or increased) prior to obtaining further tests. Table 5 lists suggested noninvasive diagnostic test for evaluation of anemia [10].

Sometimes it is difficult to differentiate iron deficiency anemia from anemia of chronic inflammation since the typical hematologic abnormalities of advanced iron deficiency occur at a later stage and both types of anemia can coexist. Table 6 will assist in analyzing equivocal results [11]. Measurement of the soluble transferrin receptor in conjunction with iron studies and ferritin, is gaining some acceptance in differentiating iron deficiency anemia from anemia of chronic inflammation.

As renal f unction decl ines in people with CKD, the Hb will progressively decline. This drop in Hb is especially noticeable as the GFR trends below 60 mL/min per 1.73 m². The anemia of CKD is typically normochromic and normocytic due primarily to a deficiency of erythropoietin production. About 50 % of nursing facility residents have a GFR below 60 mL/min per 1.73 m² and in one recent study, 60 % of residents with Stage III CKD were anemic.

Acute or chro nic immune activation can cause a disturbance of iron homeostasis that limits the av ailability of iron for erythropoiesis due to the impaired release of iron from macrophages. This disturbance in iron homeostasis is mediated by the proinflammatory cytokine interleukin-6, which increases the production of hepcidin in the liver. Hepcidin decreases duodenal absorption of iron. In addition, erythropoietic cell survival and erythropoietic cell response to EPO is decreased.

Treatment of como rbid nutritional deficiencies and hypothyroidism should be undertaken. If anemia is related to medication use, chronic bleeding, CKD, chronic inflammation, malignancy, or hemolysis, then the underlying condition should be stabilized to the extent possible and any offending drugs discontinued. Treatment options for specific types of anemia and cautions to consider are reviewed in Table 7.

Blood transfusions are generally given for acute blood loss associated with hypotension and cardiovascular compromise. For chronic anemia, blood transfusion is recommended if the Hb drops below 7 g/dL, the hematocrit decreases to 21 %, or in the presence of angina, heart failure, dyspnea, tachycardia, or hypotension.

The American College of Cardiology/American Heart Association (ACC/AHA) guidelines for the evaluation and management of HF h ave classified this condition in four stages (A-D) [14]. The first two stages (A, B) are not symptomatic stages of heart failure but defined to help practitioners identify those at risk for developing HF. The NYHA classification can be used to clarify symptom severity (Table 8).

The clinical differentiation between diastolic and systolic dysfunction although challenging, may be helpful in decision-making. A co mplete history and physical examination should be performed in residents with shortness of breath, reduced exercise tolerance, edema, or other symptoms suggestive of HF. Review of prior records may provide vital information regarding cardiovascular conditions. Current medications, use of alcohol, and/or illicit drugs and alternative therapies, as well as chemotherapy agents should also be considered as contributing factors to HF.

The manifestations of heart failure may be atypical in long–term care residents. Frail elderly may have fatigue, malaise, lethargy, declining function, or neurological symptoms such as confusion, restlessness, or sleep disturbance when they develop an exacerbation of HF. Orthopnea, dyspnea with exertion, cough or edema may be present. Gastrointestinal manifestations of HF may include anorexia, nausea, and abdominal discomfort.

Patients who h ave HFpEF (i.e., preserved EF) are more often female, have a fourth heart sound, sustained PMI, absence of jugular venous distension, absence of peripheral edema, normal heart size on chest -ray, and left ventricular hypertrophy (LVH) on the electrocardiogram (EKG). By contrast, patients with HFrEF (i.e., reduced EF) are more often male, have a third heart sound, displaced PMI, jugular venous distension, pitting edema, and Q waves on the EKG.

Electrolytes and renal fu nction should be measured regularly as hypokalemia is a common adverse effect of diuretics and may increase the risk of fatal arrhythmias or digoxin toxicity. Many residents with hypokalemia also have hypomagnesemia, which can result in an inadequate response to potassium supplementation. Hyperkalemia can be associated with ACE inhibitors, angiotensin II receptor blockers, or worsening renal function. The development of hyponatremia may be an indication of disease progression and is associated with reduced survival in the elderly with HF.

Serial chest X-rays are not recommended but monitoring weights 2–3 times a week during an exacerbation of HF is useful practice. The resident’s functional status should be monitored in addition to the physical examination with sitting and standing BP.

Close observation, a nd early detection of symptoms and signs may precede an acute HF episode by several days. Timely intervention by the practitioner (with evaluation of weights, chest X-ray, electrolytes and renal function, adjustment of therapy) and regular monitoring by nursing staff may prevent hospitalization. Records of prior cardiac investigations and echocardiograms will assist in better defining the type of HF in terms of LVEF, LVH and valvular dysfunction. A study of 156 episodes of HF in 4693 Medicare nursing facility admissions within the first 90 days of stay, reported that symptom presentation and evaluation by nursing staff at night increased the odds of rehospitalization fourfold. The presence of hypotension and delirium were predictive of death. Residents who received ACE inhibitors and orders for skilled nursing observations more than once a shift decreased the likelihood of dying by 70 % [15]. Residents with anemia (Hb <9.8 g/dL) were twofold more likely, and those with CKD (stage III or greater) were fivefold more likely to be rehospitalized from a nursing facility HF rehabilitation unit.

The followi ng reviews consensus recommendations for the management of HF and should be applied to each resident in an individualized manner [14]. The choice of pharmacologic and non-pharmacologic therapy will depend on the patient’s clinical status, goals of care, as well burden of comorbid conditions and prognosis. The suggested treatment paradigm can be based on three broadly identified groups in many facilities: the Rehabilitation Group in whom the goal is improved function and discharge; those who are frail with multi-morbidities and have an Uncertain Prognosis; and the Long–term Care Group who are frail, dependent for care needs, and expected to remain in the facility. Each recommendation should be individualized (Table 10).

Many re sidents may receive digoxin (sometimes for years) as a standard part of the treatment regimen for HF despite the presence of sinus rhythm and normal LVEF. The evidence indicates that low dose digoxin (digoxin concentration <1.0 ng/mL) may decrease mortality in HFrEF and NYHA II and III symptoms in elderly who do not have an adequate response to ACE inhibitors, beta-blockers, and diuretics.

The elderly are at increased risk of digoxin toxicity due to renal insufficiency, hypoalbuminemia, hypokalemia with hypomagnesemia, as well as drug–drug interactions. Drug interactions between digoxin and antiarrythmics, erythromycin and tetracycline can be especially problematic. Close monitoring, especially during acute illness causing dehydration, is recommended and serum concentrations should be maintained between 0.5 and 0.8 ng/ml [16].

HF can ha ve an unpredictable course and a high incidence of sudden death despite intensive medical management. Palliative care should be considered for those with refractory HF and persistence of severe and distressful symptoms such as dyspnea, fatigue, pain, sleep disturbance, and functional decline.

Smoking (90 % of cases), advan ced age, repeated pulmonary infections, prior tuberculosis, occupational or environmental causes, and alpha-1 antitrypsin deficiency are risk factors for COPD. Early identification of COPD is important since 50 % of lung function is lost by the time mild exertional dyspnea occurs and only 30 % of lung function remains when there is dyspnea at rest. All new admissions to LTC and those residents with recurrent pulmonary problems should be screened for COPD utilizing the clinical indicators listed in Table 11 [18].

On exami nation, residents may be barrel-chested, have prolonged expiration or pursed lip breathing, use accessory muscles for respiration, and have wheezing, ronchi, or distant heart sounds. The signs of cor pulmonale include jugular venous distension, hepatic congestion, pedal edema, and a loud P2 component of the second heart sound.

The clinical evaluation and review of past records may be helpful in diagnosing COPD, but the definitive method of diagnosis is by spirometry which usually measures FEV₁ (volume of air exhaled in 1 s) to FVC (forced vital capacity or total volume of air able to be exhaled). Spirometry should be performed in symptomatic individuals and may need to be repeated.

Normal: FEV ₁ /FVC ≥ 70 % or FEV ₁  ≥ 80 % of predicted

COPD: FEV ₁ /FVC ≤ 70 %

Restrictive lung disease: FEV ₁ /FVC ≥ 90 % (pulmonary fibrosis, severe kyphosis)

COPD is und iagnosed in 80 % of older adults and not all LTC facilities have bedside spirometers and their use in frail or demented residents is usually not feasible. A screening tool that uses caregivers to rate residents’ symptoms was validated in the NF by Zarrowitz et al. They report that a history of asthma, shortness of breath at rest and shortness of breath on exertion, and smoking are likely to be consistent with a diagnosis of COPD.

Other diagn ostic tests may provide useful information regarding the presence of COPD or other conditions presenting with similar signs and symptoms. A complete blood count may reveal an abnormally high Hb level due to hypoxia, and a chemistry panel may show a high bicarbonate level (respiratory alkalosis) due to hypercapnea. Even though chest X-rays are not diagnostic, they may reveal HF, bullae, pneumonia, pulmonary scarring; or low flat diaphragms, increased retrosternal airspace and a teardrop shaped heart silhouette are suggestive of COPD. An EKG may show atrial arrhythmias or right heart strain. Pulmonary consultation may be helpful if the cause of dyspnea is not clear or the resident exhibits a poor response to treatment. Clinical judgment is important since the differential diagnosis of COPD can include asthma, heart failure, brochiectasis, recurrent aspiration, ACE-inhibitor induced cough, vocal cord dysfunction, and respiratory tract tumors. The GOLD criteria of COPD severity are shown in Table 12 [19].

Since staging of COPD by spirometry criteria is not usually possible or practical in PA/LTC, clinical presentation and judgment must be utilized to guide treatment [20] (Table 13).

Encour aging smoking cessation is important at any stage of this disease; as are measures to improve nutrition, encourage physical activity and immunization with influenza and pneumococcal vaccines. Complications such as polycythemia, hypoxia, and HF should be treated, and goals of care should be discussed with the resident and family.

Pharmacological treatment should be stepwise and cumulative. Medications can reduce symptoms, increase exercise capacity, and reduce the number and severity of exacerbations; but no treatment has been shown to modify the progressive decline in lung function. Three types of bronchodilators are in common clinical use: β-agonists, anticholinergic drugs and inhaled corticosteroids.